Studies outlined are designed to elucidate the physiologic basis of immunity in trichinosis. It is proposed that (1) local acidosis and tissue hypoxia, (2) substances elaborated from degranulating or degenerating cells, and (3) altered intestinal motility which accompany antigen-evoked inflamation interfere with development or survival of intestinal stages of trichinella and are important factors in acquired resistance. The pH and pO2 in normal and inflamed intestinal tissue will be measured. Results will be correlated with those from studies on worm survival at various pO2 levels, and on oxygen uptake by worms as a function of pH. The assumption that amine excretion by intestinal stages of trichinella is an adaptive mechanism aimed at offsetting a drop in tissue pH will be examined by measuring the quantity of amines excreted and the activity of various amino acid decarboxylases of Trichinella maintained in vitro at various H plus concentrations. The myeloperoxidase-H2O2-halide system which functions in leukocytes will be examined as to its extracellular activity and its possible role in damaging or killing tissue stages of trichinella. The assumption that altered intestinal motility is responsible, in part, for worm expulsion will be evaluated by studying the changes in gastric emptying, small bowel transit, and gastrointestinal contractions in animals given primary and challenge infections, and also by altering gastric emptying and small bowel transit and observing the effects on the establishment of worms from a primary infection. Knowledge of the nature of physiologic factors involved in worm attenuation or rejection would contribute greatly to an understanding of acquired resistance to helminths and would provide a basis for developing control measures such as vaccines and antihelminthics.